Increase in adiposity is strongly associated with severe health problems and with an overall decreased longevity [2]. In particular, an increase in visceral (android) adiposity is considered [3], [4], [5], [6] the key feature of a constellation of metabolic abnormalities, known as metabolic syndrome (MS), including also glucose intolerance and insulin resistance, dyslipidaemia, and hypertension, essentially characterized by an increased cardiovascular and diabetic risk [7], [8], [9].
Men with cardiovascular diseases or diabetes mellitus (DM) or both often have erectile dysfunction (ED), probably because of shared factors impairing hemodynamic mechanisms in both the penile and systemic vascular beds [10].
Interestingly, subjects with MS, according to National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP-III; three or more 3 MS components reported in Table 1) [11] have an increasing occurrence of ED [12], [13]. Recently, the concept that MS is also associated with male hypogonadism has emerged [3], [14], [15]. Because androgen deficiency can induce ED, or might modulate clinical response to therapy with phosphodiesterase-5 inhibitors [16], [17], [18], [19], we studied the prevalence and psychobiologic characteristics of MS and its possible correlation with hypogonadism, in a large series of patients (>800) consulting for sexual dysfunction.
| |
|
|
 |
Component |
Defining level |
Prevalence in this study |
|
|
Elevated BP |
≥130mm Hg systolic BP |
76.1% |
|
|
|
or |
|
|
|
|
≥85mm Hg diastolic BP |
|
|
|
|
or |
|
|
|
|
Drug treatment for hypertension |
|
|
|
Elevated fasting glucose |
≥110mg/dl (6.1mmol/L) |
32.2% |
|
|
|
or |
|
|
|
|
Drug treatment for elevated glucose |
|
|
|
Elevated waist circumference |
>102cm |
26.8% |
|
|
Reduced HDL-C |
<40mg/dl (1.03mmol/L) |
16.6% |
|
|
|
or |
|
|
|
|
Drug treatment for reduced HDL-C |
|
|
|
Elevated TG |
≥150mg/dl (1.7mmol/L) |
36.7% |
|
|
|
or |
|
|
|
|
Drug treatment for elevated TG |
|
|
| |
|
|
NCEP-ATP-III=National Cholesterol Education Program Adult Treatment Panel III; BP=blood pressure; HDL-C=HDL cholesterol; TG=triglycerides.
2. Methods
A consecutive series of 803 patients, visiting our University Outpatient Clinic for the first time for sexual dysfunction, was studied. All patients were white. Two patients with mental retardation and seven patients unable to clearly understand the national version of Structured Interview on Erectile Dysfunction (SIEDY) [20] were excluded. The diagnosis of MS was made on the basis of NCEP-ATP-III criteria as previously described [11].
Patients were interviewed prior to the beginning of any treatment and before any specific diagnostic procedures, using the SIEDY [20], [21]. This is a 13-item interview composed of three scales, which identify and quantify components concurring to ED. Scale 1 deals with organic disorders, scale 2 with disturbances in relationship with a partner, and scale 3 with psychological traits. Scores ≥3.5 on SIEDY scale 1 are predictive of organic disturbances underlying ED with a sensitivity and specificity of about 70%. Severity of ED was analysed using SIEDY Appendix B and in particular using item 1D (see also Appendix A) [20]. Moreover, considering the National Institutes of Health definition of impotence [22] and using SIEDY Appendix B [20], we identified subjects with difficulties in maintaining, rather than achieving, an erection (when they reported an erection inadequate for penetration in <25% of cases and difficulties in maintaining erection in >25% of the occasions) and subjects with the main problem of achieving an erection (when they reported erection sufficient to penetrate in <25% of occasions) [23]. Other characteristics of the disorder were investigated using standard questions (Appendix A) [23]. Premature ejaculation (PE) and delayed ejaculation (DE), as reported by the patient, were defined according to previously described criteria [24], [25]. Hypoactive sexual desire (HSD) was assessed with item no. 14 and nocturnal/morning erections with item no. 13 of SIEDY (Appendix A) [20]. Relationship duration and frequency of sexual intercourse were assessed using specific questions (Appendix A).
Patients were asked to complete the Italian version [26] of the Middlesex Hospital Questionnaire modified (MHQ) [27]. It consists of a brief self-reported questionnaire for the screening of mental disorders, which provides scores for free-floating anxiety (MHQ-A), phobic anxiety (MHQ-F), obsessive-compulsive traits and symptoms (MHQ-O), somatisation (MHQ-S), depressive symptoms (MHQ-D), and hysterical traits and symptoms (MHQ-I).
All patients underwent a complete physical and andrologic examination, with measurement of blood pressure (mean of three measurements 5min apart, in sitting position, with a standard sphygmomanometer), height, weight, and testis volume (Prader orchidometer). Blood samples were drawn in the morning, after an overnight fast, for determination of blood glucose (by glucose oxidase method; Aeroset Abbott, Rome, Italy), total and high-density lipoprotein (HDL) cholesterol, and triglycerides (by automated enzymatic colorimetric method; Aeroset Abbott), total testosterone (TT; normal range, 10.4–34.6nmol/l), prolactin, luteinising hormone (LH), thyroid-stimulating hormone (TSH), and prostate-specific antigen (PSA; by an electrochemiluminescent method; Modular Roche, Milan, Italy), and free testosterone (FT; normal range, 37–85pmol/l; by a radioimmunoassay method; Diagnostic Products, Los Angeles, CA). We diagnosed hypogonadism when the TT level was <8nmol/l or 2.31ng/ml according to recommendations of the International Society of Andrology (ISA), International Society for the Study of the Aging Male (ISSAM), and European Association of Urology (EAU) [28].
All patients underwent penile Doppler ultrasound (PDU) examination performed before and 20min after intracavernous injection of prostaglandin E1 (PGE1; 10μg). All measurements were performed off-line by an experienced operator unaware of the clinical data. The following parameters were considered: (1) in basal condition: peak systolic velocity (Vps) and acceleration (Acc); (2) after PGE1 intracavernous injection: peak systolic velocity (Vpmax), end diastolic velocity (Edv), and resistance index (RI) [29]. The following cut-off values were used: Vps, >12.5cm/s; Acc, >1m/s2; Vpmax, >30cm/s; Edv<5cm/s; and RI≥0.9 [29].
Data were expressed as mean±SD when normally distributed and as median [quartiles] for parameters with nonnormal distribution, unless otherwise specified. Differences between more than two groups were assessed with one-way ANOVA or Kruskal–Wallis test, whenever appropriate. Unpaired two-sided Student t tests were used for comparison of means of normally distributed parameters. In all other cases, the Mann–Whitney U test was used for comparisons between groups. Relative risk and 95% confidence intervals were calculated for association of categorical parameters, and the χ2 test was used for comparisons. Stepwise multiple linear regression or logistic multiple regression were applied for multivariate analysis, whenever appropriate. All data were adjusted for confounding factors such as patient or partner age or waist circumference. All statistical analyses were performed on SPSS for Windows 12.0.
3. Results
Among the 803 patients studied (mean age, 53.6±12.1 yr), 749 (93.3%) reported ED, 294 (36.6%) HSD, 206 (25.7%) PE, and 39 (4.8%) DE. The diagnosis of MS was made when three or more MS components (NCEP-ATP-III criteria) shown in Table 1 were present. In this population, 118 (14.7%) patients had no MS components, 244 (30.4%) had one MS component, 205 (25.5%) had two MS components, and 236 (29.4%) had MS (137 patients [17.0%] had three components and 99 [12.4%] had four or more MS components). Patients with MS were significantly older than the rest of the sample (58±9 vs. 52±13 yr; p<0.0001) and they also showed a higher prevalence of stable relationships living together with their partners (77.8% vs. 68.8%; p<0.01). However, this difference did not retain statistical significance after adjustment for age.
The proportion of patients with relationship duration longer than 10 yr was significantly higher among those with MS (84.2% vs. 68.1%; p<0.0001), even after adjustment for the patient's or partner's age. Conversely, the SIEDY scale 2 score, which explores other relational factors involved in the pathogenesis of ED, was not significantly different in patients with or without MS.
Considering intrapsychic factors, patients with MS showed a significantly higher score in the MHQ-S scale (4.73±2.6 vs. 4.17±2.7, respectively; p=0.011). In particular, patients affected by four or more MS components had a higher MHQ-S score (p<0.01 at ANOVA; Fig. 1A) when compared to patients without MS components. The difference retained significance even after adjustment for age. Conversely, the SIEDY scale 3 score, which explores intrapsychic factors in the pathogenesis of ED, was not significantly different in patients with or without MS.
Fig. 1. (A) Relationship between somatisation (as expressed by Middlesex Hospital Questionnaire-Somatisation [MHQ-S] score) and the number of metabolic syndrome (MS) components (mean and 95% CI). (B) Relationship between organic erectile dysfunction (ED; Structured Interview on Erectile Dysfunction [SIEDY] scale 1 score) and the number of MS components (mean and 95% confidence interval [CI]). MS components were calculated accordingly to National Cholesterol Education Program Adult Treatment Panel III criteria: blood pressure (BP) ≥130/85mm Hg or medication; glycaemia ≥110mg/dl (6.1mmol/L) or previously diagnosed diabetes mellitus; waist circumference >102cm; high-density lipoprotein cholesterol (HDL-C) <40mg/dl (1.03mmol/l) or medication; triglyceride (TG) level ≥150mg/dl (1.7mmol/L) or medication. *p<0.005 **p<0.0001 versus 0 metabolic syndrome components.
The SIEDY scale 1 score, which reflects the organic domain of ED [20], progressively increased as a function of the number of MS components involved (Fig. 1B; B=0.54±0.05; p<0.0001, after adjustment for age).
The overall prevalence of MS and the numbers of MS components progressively increased as a function of age, peaking in the 50–59-yr-old group (37.8%; Table 2). Among patients with MS 96.5% reported ED, 39.6% HSD, 22.7% PE, and 4.8% DE. No significant difference, after adjustment for age, was observed in the prevalence of ejaculation disorders or in hypoactive sexual desire in patients with or without MS. Conversely, patients with MS showed a greater severity of ED when compared to the rest of the sample. The proportion of men lacking erection during intercourse in the majority (>75%) of occasions (as assessed by question no. 1D of SIEDY Appendix B; see also Appendix A) was 10.3% in MS patients versus 5.6% in the rest of the sample (p=0.020). Patients with MS reported a higher prevalence of problems in achieving an erection and a lower prevalence of difficulties in maintaining it (71.7% vs. 55.5% and 28.3% vs. 44.5%, respectively; both p<0.0001). Furthermore, a progressive onset of the disorder was observed more often in patients with MS when compared to those without MS (81.2% vs. 68.9%, respectively; p<0.001). Finally, a reported reduction of nocturnal/morning erections was present in 78.6% of patients with MS and in 67.8% of rest of the sample (p<0.005). All these differences were confirmed at multivariate analysis after adjustment for age.
| |
|
|
|
Age (yr) |
No. of MS components (%) |
MS, ≥3 components (%) |
|
|
|
0 |
1 |
2 |
3 |
4 |
5 |
|
|
|
<30 |
67.7 |
16.1 |
16.1 |
0 |
0 |
0 |
0 |
|
|
30–39 |
36.4 |
38.6 |
15.9 |
6.8 |
2.3 |
0 |
9.1 |
|
|
40–49 |
19.4 |
37.4 |
22.3 |
9.4 |
9.4 |
2.2 |
20.9 |
|
|
50–59 |
7.7 |
27.2 |
27.2 |
19.1 |
15.4 |
3.3 |
37.8 |
|
|
60–69 |
6.3 |
27.8 |
29.0 |
25.0 |
9.1 |
2.8 |
36.9 |
|
|
>69 |
6.4 |
34.0 |
31.9 |
17.0 |
8.5 |
2.1 |
27.7 |
|
| |
|
|
MS=metabolic syndrome; NCEP-ATP-III=National Cholesterol Education Program Adult Treatment Panel III.
Basal and dynamic (after PGE1 stimulation) peak systolic velocity at PDU showed a progressive decline as the numbers of MS components increased (Fig. 2A and B); this trend was significant even after adjustment for age (B=−0.79±0.23 and −2.23±0.69cm/s, respectively; both p<0.001). Conversely, no significant association was observed between the number of MS components involved and other PDU parameters, such as Acc, Edv, and RI. At logistic regression analysis, considering MS components as putative predictors for pathologic dynamic peak systolic velocity (i.e., Vpmax<30cm/s), triglycerides, hyperglycaemia, and hypertension were all significantly related to Vpmax (p=0.03, 0.03, and 0.005 respectively; Fig. 2C).
Fig. 2. Effect of metabolic syndrome (MS) components on the penile Doppler ultrasound parameters in patients with MS-associated sexual dysfunction. Relationship between basal (Vps; panel A) and dynamic (Vpmax; panel B) penile peak systolic velocity and the number of MS components (mean and 95% confidence interval [CI]). (C) Odds ratio (95% CI) for pathologic Vpmax (<30cm/s), as detected by logistic regression analysis considering MS components as putative predictors. MS components were calculated accordingly to criteria outlined in Fig. 1. BP=blood pressure; HDL-C=HDL cholesterol, TG=triglycerides. *p<0.05, **p<0.005, ***p<0.0001 versus 0 metabolic syndrome components.
Among patients with MS, the prevalence of hypogonadism was 11.9%; it was 3.8% in the rest of the sample (p<0.0001). A substantial reduction in circulating FT levels (B=−3.5±1.37pmol/l; p<0.02, after adjustment for age) was also associated with MS (34.9±14.8 vs. 40.5±13.9pmol/l; p<0.0001). The association of MS with circulating androgens is summarized in Fig. 3 A. Circulating TT decreased as the number of MS components increased (B=−1.35±0.182nmol/l; p<0.0001, after adjustment for age). Accordingly, the relative risk for hypogonadism was significantly higher in patients reporting three or more risk factors for MS (Fig. 3B). At logistic regression analysis, considering components of MS as putative predictors for hypogonadism, waist circumference, and hyperglycaemia, but not other factors, resulted in a significant association with low TT level (p=0.005 and 0.02 respectively; Fig. 3C). Among patients with MS, those with hypogonadism showed higher body mass index (BMI) and waist circumference (Table 3). They also showed higher LH and FSH and lower FT levels when compared to eugonadal patients with MS (B=3.5±1.2, 11.6±2.5U/l and −10.6±3.1pmol/l, respectively; all p<0.001, after adjustment for confounding factors such as waist circumference and age), which was coupled to a lower testis volume (Table 3). No difference was observed in ED severity or PDU parameters between eugonadal or hypogonadal patients with MS. Among patients with MS, hypogonadism was associated with lower sexual desire, as assessed by question no. 14 of SIEDY, higher depression scores, as assessed by the MHQ-D scale, and lower frequency of intercourse (Table 3). The association between loss of sexual desire and circulating testosterone retained statistical significance even after adjustment for MHQ-D score (adjusted r=–0.205; p<0.005). All these differences were confirmed after adjustment for other confounding factors.
Fig. 3. Effect of metabolic syndrome (MS) components on the prevalence of hypogonadism in patients with MS-associated sexual dysfunction. (A) Relationship between total testosterone (TT) and the number of MS components (mean and 95% confidence interval [CI]). (B) Relative risk (95% CI) for hypogonadism (TT<8nM) accordingly with the number of MS components. (C) Odds ratio (95% CI) for hypogonadism (TT<8nM) as detected by logistic regression analysis, considering MS components as putative predictors. MS components were calculated accordingly to NCEP-ATP-III criteria as indicated in Fig. 1. BP=blood pressure; HDL-C=HDL cholesterol, TG=triglycerides. *p<0.0001 versus no metabolic syndrome components.
| |
Table 3. |
|
|
|
Hypogonadal |
Eugonadal |
p |
|
|
Age (yr) |
59±9 |
57±8 |
0.47 |
|
|
BMI (kg/m2) |
32.1±4.9 |
30.1±4.7 |
0.03 |
|
|
Waist circumference (cm) |
112.1±12.8 |
106.8±11.9 |
0.03 |
|
|
Testis volume (ml) |
16.1±5.8 |
20.1±3.7 |
0.0001 |
|
|
Luteinising hormone level (U/l) |
5.8 (3.5–11.9) |
3.9 (2.7–5.3) |
0.002 |
|
|
Follicle-stimulating hormone leve (U/l) |
12.1 (4.3–24.8) |
5.1 (3.4–8.3) |
0.003 |
|
|
Free testosterone level (pmol/l) |
24.2±11.9 |
36.9±14.5 |
0.0001 |
|
|
HSD (%) |
66.7 |
33.3 |
0.003 |
|
|
Depression symptoms (MHQ-D score) |
7.2±3.5 |
5.5±3.2 |
0.03 |
|
|
Frequency of intercourse >1/mo (%) |
55.6 |
78.7 |
0.009 |
|
| |
|
|
Hypogonadal patients had total testosterone levels <8nM.
Values are reported as mean±standard deviation when normally distributed, as median [quartiles] for parameters with nonnormal distribution or as percentage when categorical. All parameters retained significance after adjustment for confounding factors as age or waist circumference.
NCEP-ATP-III=National Cholesterol Education Program Adult Treatment Panel III; BMI=body mass index; HSD=hypoactive sexual desire; MHQ-D=Middlesex Hospital Questionnaire modified, depression sympton score.
No other differences were observed between patients with and without MS for all of other hormonal parameters measured.
4. Discussion
MS (visceral obesity, high triglycerides/low HDL cholesterol, hyperglycaemia, and hypertension) has been proposed as identifying individuals with increased metabolic and cardiovascular risk. We now report its challenging association with male sexual health disorders and define its hormonal and psychobiologic correlates.
Although the relationship between cardiovascular risk factors and impaired sexual health has been known for at least two decades, in this study we report the specific association between male sexual dysfunction and MS. Recognising MS-associated sexual dysfunction (MSASD) might help physicians in identifying, among those reporting sexual dysfunction, high-risk individuals, who could be candidates for specific lifestyle (such as weight loss and physical exercise) and therapeutic interventions, beyond those specifically designed for sexual dysfunction. It could be speculated that correction of some metabolic parameters could lead to an improvement of sexual function in patients with MSASD.
We found that, among patients with sexual dysfunction, those with MS are characterized by the worst erectile function, essentially due to impairment in penile blood flow. Accordingly, they report a prevalent difficulty in obtaining versus maintaining erection, a gradual onset of the disorder, and a decreased number of nocturnal erections, all of which were demonstrated to be associated more with an organic than a psychogenic origin of ED [23]. In addition, SIEDY scale 1 scores, which reflect the organic origin of ED [20], progressively increase as the different components of MS increase. Among the factors characterising MS, those more directly associated with deteriorating penile blood flow are hypertension and glucose sensitivity (as mirrored by increased glycaemia and triglyceride levels). This finding is not surprising because it is known that impaired glucose control is a risk factor for the development of atherosclerotic vascular disease [30], [31], [32], with deleterious effects also on the penile vascular bed [33].
Although MS is not characterized by any specific symptom, we found that patients with MSASD have great somatised anxiety. Somatisation, which is the expression of physical symptoms in the absence of medically explained physical illness, might be viewed as a part of maladaptive thought or behaviour—or just as a dysfunctional response—to the sexual dysfunction itself, which is often unaccepted or unrecognised in its organic basis. It should be considered that many of the MS components are not recognised as “diseases” by the general population nor by the medical profession in general (e.g., excess abdominal fat or mild hypertension). When individuals avoid dealing with their dysfunction and its origin, they inadvertently prolong and aggravate the situation and the distress [34]. Hence, it is important to correctly recognise and identify MSASD to decrease or suppress this denial behaviour and its accompanying somatisation symptoms.
MSASD is far more common in the older man, peaking at 50–59 yr. Interestingly, even after adjustment for confounding factors as the patient's or partner's age, MSASD is more common in prolonged (>10 yr) couple relationships. It could be speculated that men with relationships of shorter duration could have a greater awareness of body shape and this could contribute to more effective weight control, through physical activity and healthier eating habits, preventing MS. Also, couples with a more recent relationship may engage more frequently in sexual activity, which by itself has been shown to decrease cardiovascular problems [35]. On the other hand, in long-term established couples, MSASD could interrupt a sustained period of successful and comfortable sexuality and relationship.
In a subset of MSASD patients, MS is further complicated by an overt hypogonadism (TT level <8nM or 2.31ng/ml). The diagnosis of MS (three or more NCEP-ATP-III criteria fulfilled) was associated with a more than 3-fold increase in the prevalence of hypogonadism. The prevalence of hypogonadism among those with all five NCEP-ATP-III criteria was 10 times higher than in subjects with no metabolic abnormalities. This is not an unexpected finding because the correlation between MS and low T level is recognised [14], [15]. In our sample, the major determinants of metabolic syndrome-associated hypogonadism (MSAH) are increased waist circumference (visceral adiposity) and hyperglycaemia. Understanding the reasons for these associations is beyond the scope of this study and several dedicated reviews have been recently published on this topic, highlighting the predominant role of obesity that leads to an increase in leptin secretion, resulting in reduced testosterone production [14], [15], [36], [37]. However, it is interesting to note that MSAH in our series is characterized by a lower FT level and by a primary testicular failure, which is demonstrated by increased gonadotropin levels along with a decreased testicular size. Interestingly, a recent report indicates that decreased insulin sensitivity is coupled to a decreased testicular production of testosterone, characterized by a decreased responsiveness to human chorionic gonadotropin (HCG) stimulation [38]. It should be recognised that recent studies focused on the possibility that hypogonadism associated with MS could play an important role in the endothelial damage leading to cardiovascular and erectile problems [14]. However, it should be emphasised that these findings have been questioned and data are inconclusive [39]. Accordingly, we did not find any difference in the ED severity and PDU parameters comparing eugonadal and hypogonadal patients with MS.
Patients with MSAH show lower sexual desire and greater depressive symptoms, with the obvious deleterious consequences of both factors on the already compromised sexual function. The final result is that the frequency of sexual intercourse reported by those with MSAH is even lower than that reported by patients with MSASD.
5. Conclusion
Among patients with sexual dysfunction, those with MS are characterized by the worst erectile function. Recognising MSASD is not only important for improving their sexual life, but also for alerting patients and physicians on the potential cardiovascular and metabolic risks often associated with this condition. In addition, recognising MSAH is equally important for the treatment of hypogonadism, which, without the appropriate therapy, can further compromise both sexual and general health, possibly sustaining a vicious circle and worsening the patient's general condition.
Editorial Comment
Alberto Briganti, Department of Urology, Università Vita-Salute, Milan, Italy
Metabolic syndrome (MS) represents a high risk medical condition. Despite different definitions, all of them have common requirements, including central obesity, insulin dysregulation, abnormal lipid profile and borderline or overt hypertension. Since these constitute established risk factors for erectile dysfunction (ED) [1], a high prevalence of ED is to be expected among patients with MS [2].
Corona et al. are to be congratulated for their excellent report. Their study emphasizes the need to assess MS in men with sexual dysfunctions. Among patients with sexual dysfunctions, those with MS showed higher prevalence of ED, worse overall erectile function and higher anxiety, which might in turn affect erectile performance, compared to a population without MS. Moreover, confirming previous evidence[2], ED severity was directly related to the number of MS components. These findings deserve further comments. Indeed, patients with multiple MS components should be considered at high risk of ED. In this context, endothelial function impairment seems to play a key role. Severity of endothelial dysfunction increases with the number of metabolic components and progressively affects erectile function of patients with MS [2]. However, this hypothesis cannot be confirmed in the study by Corona et al. In fact, tests assessing endothelial function were not performed. Instead, routine diagnostic PGE-1 induced cavernosal dilation, which mainly represents an endothelium-independent vasodilation, was measured. However, their findings emphasize the need for a prospective evaluation of patients with ED and MS. Indeed, small penile vascular vessels could represent the first target of a systemic atherosclerotic process, which might further involve larger vessel if a chronic exposure to vascular risk factors is maintained [3]. In this context, life style modifications may play a crucial role, as it has been shown that simple dietary changes might be effective “per se” in reducing prevalence of ED in patients with MS [4]. Further studies are needed to address this issue. Finally, the study by Corona et al. confirms previous studies reporting a high prevalence of hypogonadism in patients with MS, which could partially explain the high prevalence of hypoactive sexual disorder (40%) in the same subset of patients [5]. This is again of extreme importance, as recognizing and treating MS-associated hypogonadism might exert a beneficial effect on many parameters, including body mass, insulin secretion, lipid profile and blood pressure [5], [6]. This, in turn, may modify the overall patient vascular profile.
In conclusion, prospective longitudinal studies and predictive tools for patient outcome are thus urgently needed, in order to correctly counsel patients with ED and multiple vascular risk factors (such as those with MS), regarding the risk of developing major cardiovascular accidents.
Acknowledgements
We would like to thank Csilla Krausz, Angela Magini, Alessandra D. Fisher, Andrology Unit of the University of Florence, and M. Bartolini, Radiology Unit of the University of Florence, for their helpful clinical collaboration during the course of the study. This study was partially supported by a grant from Centro di Ricerca Trasferimento ad Alta Formazione MCIDNENT of the University of Florence.
Appendix A. Main questions applied during patient's interview
1. SIEDY questions#13 Does it ever occur to you to wake up with an erection?
How often did it happen in the last three months? How often did it happen in the past?0 The patient reports spontaneous nocturnal/morning erections, with the same frequency previously observed; 1 Nocturnal/morning erections are present, but their frequency during the last three months is somewhat lower than that observed previously; 2 The frequency of nocturnal/morning erections of the last three months is reduced by at least 50%; 3 No nocturnal/morning erections are present.
0.Yes, regularly
1.Less frequently than in the past
2.Only occasionally
3.Never
#14 Did you have more or less desire to make love in the last three months?
Was your desire increased or reduced when compared to the past?0 when the patient's desire is unmodified or increased; 1 If desire is moderately reduced, in less than 50% of potential occasions; 2 If desire is reduced in more than 50% of potential occasions; 3 If the patient has had no desire to make love. The question investigates only the patient's, and not the partner's, desire. The last three months should be considered.
0.Unmodified or increased desire
1.Desire present but moderately reduced
2.Desire remarkably reduced
3.Desire never present
2. SIEDY appendix B questions
#1 Describe what happens during sexual intercourse: do you have an erection? Is it a complete erection?
Is it sufficient for penetration? How often?The patient has to describe the erectile problem answering the previous question. The interviewer should reformulate the patient's answers to confirm that there was no misunderstanding. The description of the problems refers to the last three months: sometimes ≤25% of cases, quite often=26–50%, often=51–75% and always ≥75%.#1D Absent erection
0.Sometimes
1.Quite often
2.Often
3.Always
3. Other questions
1.How long is the relationship with your partner?
0.lower than 1 year
1.between 1–5 years
2.between 5–10 years
3.more than 10 years
2.During the last three months how many sexual attempts per month did you have?
0.no attempts
1.1–2 attempts/month
2.3–7 attempts/month
3.8 or more attempts/month
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Giovanni Coronaae1, Edoardo Mannuccib1, Claude Schulmanc, Luisa Petronea, Riccardo Mansania, Antonio Cilottia, Giancarlo Balerciad, Valerio Chiarinie, Gianni Fortia, Mario Maggia
a Andrology Unit, Department of Clinical Physiopathology, University of Florence, Florence, Italy
b Diabetes Section Geriatric Unit, Department of Critical Care, University of Florence, Florence, Italy
c University Clinics of Brussels, Erasme Hospital, Department of Urology, Brussels, Belgium
d Endocrinology Unit, Polytechnic University of Marche, Ancona, Italy
e Endocrinology Unit, Maggiore-Bellaria Hospital, Bologna, Italy
1 G. Corona and M. Mannucci contributed equally to the paper.
Accepted 21 February 2006 published online 15 March 2006.Please log-in or register in order to submit comments. Powered by AkoComment! |
